论文部分内容阅读
目的 探讨癫痫发病的分子机制。方法 采用原位杂交技术 ,研究了马桑内酯致痫大鼠大脑皮层、海马 N-甲基 - D-天门冬氨酸受体亚单位 1(NMDAR1) m RNA表达的变化。结果 马桑内酶致痫大鼠顶叶大脑皮层及海马齿状回 NMDAR1m RNA水平显著高于生理盐水对照组 (P<0 .0 1,P<0 .0 5 )。结论 马桑内酯上调脑组织内NMDAR1m RNA水平 ,此可能是其致痫及惊厥易感性增加的分子机制之一
Objective To investigate the molecular mechanism of epilepsy. Methods The in situ hybridization technique was used to study the changes of NMDAR1 mRNA expression in cerebral cortex and hippocampus of rats with epilepsy induced by. Results The level of NMDAR1m RNA in the parietal cortex and hippocampal dentate gyrus of rats with epilepsy was significantly higher than that of the saline control group (P <0.01, P <0.05). Conclusion Coriatolactone upregulates the level of NMDAR1m RNA in brain tissue, which may be one of the molecular mechanisms of its increased susceptibility to epilepsy and seizure